Mononuclear cells infiltrating the granulomatous lesions in the arterial wall then contribute to producing mediators, such as Platelet-Derived Growth Factor (PDGF) (6) and endothelin-1 (7, 8), triggering the proliferation and migration of VSMCs from the media to the intima, which, together with the production of proteins of the extracellular matrix (collagen-1, collagen-3 and fibronectin), contribute to intimal hyperplasia leading to vascular occlusion and ischemic signs of GCA (5, 9). The gene discussed is EDN1; the disease is temporal arteritis.